Enhanced depletion of MLL-fusion proteins in acute leukemia: potential for improved therapeutic outcomes
- Standort
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Deutsche Nationalbibliothek Frankfurt am Main
- Umfang
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1 Online-Ressource.
- Sprache
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Englisch
- Erschienen in
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Enhanced depletion of MLL-fusion proteins in acute leukemia: potential for improved therapeutic outcomes ; volume:13 ; number:1 ; day:16 ; month:8 ; year:2024 ; pages:1-5 ; date:12.2024
Experimental hematology & oncology ; 13, Heft 1 (16.8.2024), 1-5, 12.2024
- Urheber
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Che, Noelia
Cantilena, Sandra
Looi-Somoye, Remi
Sundar, Danesh
Fung, Kent
Boer, Jasper de
Williams, Owen
- Beteiligte Personen und Organisationen
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SpringerLink (Online service)
- DOI
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10.1186/s40164-024-00556-w
- URN
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urn:nbn:de:101:1-2411032116579.803036564360
- Rechteinformation
-
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Letzte Aktualisierung
- 15.08.2025, 07:24 MESZ
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Beteiligte
- Che, Noelia
- Cantilena, Sandra
- Looi-Somoye, Remi
- Sundar, Danesh
- Fung, Kent
- Boer, Jasper de
- Williams, Owen
- SpringerLink (Online service)
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A novel spliced fusion of MLL with CT45A2in a pediatric biphenotypic acute leukemia
circRNA circAF4 functions as an oncogene to regulate MLL-AF4 fusion protein expression and inhibit MLL leukemia progression
MLL oncoprotein levels influence leukemia lineage identities
RNA binding proteins in MLL-rearranged leukemia
IMPDH inhibition activates TLR‐VCAM1 pathway and suppresses the development of MLL‐fusion leukemia
A novel spliced fusion of MLL with CT45A2 in a pediatric biphenotypic acute leukemia
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MLL-fusion-driven leukemia requires SETD2 to safeguard genomic integrity
Progenitor like cell type of an MLL-EDC4 fusion in acute myeloid leukemia
A novel spliced fusion of MLL with CT45A2in a pediatric biphenotypic acute leukemia
circRNA circAF4 functions as an oncogene to regulate MLL-AF4 fusion protein expression and inhibit MLL leukemia progression
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IMPDH inhibition activates TLR‐VCAM1 pathway and suppresses the development of MLL‐fusion leukemia
A novel spliced fusion of MLL with CT45A2 in a pediatric biphenotypic acute leukemia
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